Animal Diseases Final (Presentations) + More

Bluetongue

1. True/False: Bluetongue is a zoonotic disease. 2. True/False: Bluetongue is spread by direct contact.

Polysaccharide Storage Myopathy (PSSM)

What type of testing is necessary to diagnose a horse suspected of having PSSM1? a. Bacterial culture b. Virus Isolation/PCR c. Genetic d. Fecal egg count What is "tying-up"/exertional rhabdomyolysis? Muscle tremors following exercise.

Primary photosensitization

• Occurs when photodynamic agent is either ingested, injected, or absorbed through the skin • Agent enters the systemic circulation in its native form, where it results in skin cell membrane damage after the animal is exposed to ultraviolet light • Ex. hypericin from St. John's wort and fagopyrin from buckwheat

Gastrointestinal Helminthiasis Cont.

• Signs can include: • Anemia (for specific parasites that are hemophagic) • "Bottle jaw" (edema under mandibles) • Develops secondary to low protein (loss through GI or with severe blood loss) • Most common in ruminants • Diarrhea • Poor growth, decreased feed conversion, weight loss • Decreased production (milk, meat, fiber, eggs) • Death •Some parasite eggs can remain viable in soil for years •Diagnosis through identification of parasite which typically involves: • Worm segments in feces • Adult worms on post-mortem • Identify oocytes/ova (eggs) on fecal flotation

Hydrogen Sulfide Gas

• Toxic gas produced by anaerobic bacterial decomposition of feces and feed • Low concentration in most swine barns • When slurry is agitated or improperly moved = large gas pockets can be released and increase concentrations to dangerous levels • Irritation of airways and breathing difficulties, muscular spasms, disorientation -> seizures -> death • Can affect workers as well

Obstruction with Urinary Stones

• Typically male animals • Penile sigmoid flexure and vermiform appendage (urethral process) in sheep and goats • Sigmoid flexure in cattle • Can be a partial or intermittent obstruction • May see blood in urine, straining to urinate (may look like straining to defecate = tenesmus), vocalization, swelling around prepuce, anorexia • Can lead to bladder rupture • Straining can lead to rectal prolapse • Results in metabolic imbalances that can be fatal

Taenia hydatigena

•Dog tapeworm • Sheep and goats are intermediate hosts •Larvae penetrate GI wall -> migrate to liver or surface of GI were form large fluid, filled cysts = cysticerosis • Clinical disease only occurs with large numbers = liver damage •No treatment •Prevent by limiting exposure to dog feces

Haemonchus contortus

•Most important nematode of small ruminants in much of US, especially in warmer climates • "Barber pole worm" •Direct life cycle •Adult worms attach to abomasal mucosa and feed on blood -> anemia, edema, death

Ineffective Deworming Schemes

•Opportunistic •Deworming only when handling for other procedures •Salvage • Save lives of heavily parasitized animals • If wait to treat, production has already been compromised •Suppressive •Deworming at regular intervals, usually every 2-4 weeks • Labor intensive, expensive, drug resistance quicker

Nipah Virus (NiV)

Please describe two routes of transmission of Nipah Virus from bats to humans. Bats eat fruit that pigs eat, then humans are in contact with the pig Bats eat fruit that pigs eat, then humans eat the pig Bats eat fruit which humans then eat Bats eat date palm tree sap which humans then eat Please list 2 clinical signs of Nipah Virus in a pig and 2 symptoms of NiV in a human. Pig: severe coughing, dyspnea, twitching, ataxia, convulsions Human: mild cough, fever, headache, encephalitis

Herpesvirus B in Rhesus Macaques

Where is the best source to obtain Herpesvirus B negative monkeys? A. Their native country B. SPF certified colonies C. AZA accredited zoos D. GFAS accredited sanctuaries True or false, most infected monkeys show major symptoms within a week of infection? False, most monkeys show little to no symptoms.

Taenia solium

Zoonotic parasite of pigs • Endemic in large areas of Latin America, Asia and sub-Saharan Africa • Adult cestode occurs in the small intestine of humans (definitive host) causing taeniosis • Pass eggs in feces, no tissue cysts • Larval stage (cysticercus) occurs in striated muscles, subcutaneous tissues and central nervous system of pigs (intermediate hosts), causing cysticercosis • Do not pass eggs in feces, have tissue cysts • Ingestion of eggs shed in faeces of infected humans will result in cysticerosis in both pigs and humans • Humans also infect by eating larval stage in contaminated pork, but that results in taeniosis •Focus is on preventing infection •Humans •Hygiene/safe waste disposal • Meat inspection • Cook meat to appropriate temperature •Pigs • Prevent exposure to human feces (use as fertilizer, pig access to latrines, etc.)

Porcine Cystitis-Pyelonephritis Complex Cont.

pH of urine increases (more basic) due to cleavage of urea into ammonia by bacterial urease enzymes • Increased urine pH: • Enhances pathogenic bacterial growth • Inhibits growth of competitive microflora • Inflames mucosal surface of urogenital tract • Promotes precipitation of urinary salts and crystals, particularly struvite • Increase inflammatory changes in bladder mucosa • Provide a surface for bacterial growth and protection from antibiotics and host defense mechanisms •Hypothesized that damage to ureteric valves secondary to bacterial products may predispose to (upstream) pyelonephritis • Low morbidity, but relatively high mortality • Increased frequency in advanced-parity (6+) sows • Severe cases = kidneys fail to function and sow dies • Signs = anorexia with weight loss/decreased production, hematuria (blood in urine), foul smell to urine, increased frequency of urination • Typically marked inflammation in bladder, ureters, and kidneys with exudate (pus) and tissue ulceration and necrosis •Diagnose with urinalysis & culture • Blood, bacteria, crystals, increased pH •Treatment •Antibiotics early in disease course •Urine acidifiers (oral feed grade citric acid) •Control & prevention • Improve hygiene •Ensure water access •Culling program for older sows

Gastrointestinal Helminthiasis

• 100's of worm species recognized in wild and domestic animals • Nematodes (roundworms) are most significant in number and economic impact in domestic species • Cestodes (tapeworms) also common • Generally less of a concern in confinement operations • Most US commercial pigs raised indoors, slatted floors prevent re-ingestion of infected feces • Most poultry and swine operations use all-in/all-out groups • More of a concern with free range/extensively reared animals •Direct fecal-oral transmission most common •Some (including all cestodes) have indirect life-cycle with invertebrate intermediate hosts • Infections thrive with • Poor sanitation • Increased stocking density & overgrazing •Hospitable environment for parasite eggs (moist, warm) • Overuse of anti-parasiticides...builds resistance in parasite population

Iron Toxicity in newborn pigs

• After iron injection during processing • Die rapidly or up to 4 days later • Rare • Predisposing factor is low vitamin E or selenium in sow -> piglets deficient • 3 forms • Severe muscle necrosis at site of injection -> release of a lot of potassium from dying cells -> cardiac arrhythmia and death • Block ability of white blood cells to destroy invading bacteria -> die of enteritis, likely E. coli • Causes abnormal calcium metabolism in tissues -> hard swelling at site of injection and calcification of other body systems

Bovine Anaplasmosis Cont

• After recovery, cattle remain chronically infected carriers but are generally immune to further clinical disease •Diagnosis • Microscopic examination blood films • A marginale inclusions are usually located toward margin of infected RBC, whereas A centrale inclusion bodies are located more centrally • Microscopically, infection becomes visible 2-6 wk after transmission • Also PCR and serology • Treatment = antibiotics • Carrier state may be eliminated with long course of antibiotics • Vaccine not currently available in US • Vector control is necessary

PCVD Cont

• Also associated with • Reproductive failure (late term abortions & stillbirths) • Subclinical infection linked with stunted growth • +/-"porcine respiratory disease complex" • Increases severity of pneumonia caused by other agents • +/-"porcine dermatitis and nephropathy syndrome" • Immune-mediated disease, in pigs 8-18 wks old, high case fatality • Blotchy, purple skin on hind legs and perineum and kidney disease •Diagnose based on clinical signs with demonstration of virus within lesions (immunochemistry/immunofluorescence) • PCV2 is ubiquitous & virus replicates in individual pigs for weeks to months • Thus, isolation of virus, detection of PCV2 DNA in serum or tissues, or detection of PCV2 antibodies in serum is not sufficient to establish a diagnosis • Control includes culling affected pigs, treating secondary bacterial infections, and vaccination (can reduced severity and incidence of disease)

Equine Granulocytic Ehrlichiosis

• Anaplasma phagocytophilum • Obligately intracellular Gram-negative bacteria • In cytoplasmic vacuoles of neutrophils and occasionally eosinophils • In the order Rickettiales • Naturally occurring infections have been seen in horses, burros, dogs, llamas, and rodents • Transmission = vector borne • Frequently infects horses wherever tick vector (Ixodes sp) is present • Zoonotic • Human exposure occurs through tick bites, and not by direct transmission from horses to people • Severity of signs varies with age of horse and duration of illness • Horses <1 yr old may have a fever only • 1-3 yr old develop fever, depression, mild limb edema, and ataxia • Adults exhibit fever, partial anorexia, depression, reluctance to move, limb edema, petechiation (small/pinpoint bruises in skin and mucous membranes), and jaundice (yellow mucous membranes/conjunctiva/sclera) •Diagnosis •Demonstration of characteristic intracellular inclusion bodies in a standard blood smear is diagnostic • Inclusions are few during first 48 hr and increase to 30%-40% of circulating neutrophils at days 3-5 of infection • Also PCR or serology • Treatment with antibiotics • Tick control measures are mandatory •No vaccine exists

African Swine Fever

• Asfarviridae, enveloped DNA virus • Highly resistant to a wide pH range and to a freeze/thaw cycle • Can remain infectious for months at room temperature or when stored at 4°C • Can remain viable in unprocessed pig meat for several weeks • Endemic in South-Saharan Africa • US has never had an outbreak • Only affects swine • In Africa, virus produces inapparent infection in 2 species of wild swine (warthog and bushpig) and in soft tick (Ornithodoros moubata)

Anthrax

• Bacillus anthracis •Gram positive rod • Resistant, infective spores can survive >15 years in environment • Worldwide distribution • Absent from some countries in western Europe, north Africa, and in US east of Mississippi • Enzootic in west Texas and northwest Minnesota; sporadic in south Texas, Montana, eastern North and South Dakota; and only occasionally seen elsewhere • Most common in wild and domestic herbivores (eg, cattle, sheep, goats, camels, antelopes) •Transmission by ingestion, wound contamination, or inhalation • Grazing animals become infected when ingest spores from soil or contaminated feed • Biting flies may mechanically transmit spores • Contaminated meat consumption reported in pigs, dogs, cats, mink, wild carnivores, and people •Vegetative bacilli released from an animal after death (by carcass bloating, scavengers, or necropsy), oxygen in air induces sporulation • Field necropsy is discouraged = potential for blood spillage -> vegetative cells exposed to air -> large numbers of spores produced

Rabbit Hemorrhagic Disease

• Caliciviruses, RNA viruses • RHDV and RHDV2 cause rabbit hemorrhagic disease • RHDV affects wild and domestic European rabbits (Oryctolagus cuniculus) • Endemic to Australia, New Zealand, Cuba, parts of Asia and Africa, as well as most of Europe • RHDV2, which first emerged in Europe in 2010, affects European rabbits, hares (Lepus spp.), wild American cottontails (Sylvilagus spp.) • In early 2020 an outbreak of RHDV2 emerged in wild and domestic rabbits in the southwestern U.S. and northern Mexico (3rd US outbreak since 2018) • Related virus causes European brown hare syndrome • Transmission through direct contact, inhalation, ingestion, and fomites that have been contaminated with rabbit bodily fluids • Highly contagious • Very high morbidity and mortality (~80%) • Rabbits of all ages affected • RHDV has been used to help control excessive numbers of non-native European rabbits in Australia • Incubation period 1 to 5 days • Often die suddenly without showing any signs • May show fever, inappetence, lethargy, convulsions, respiratory distress, jaundice, petechia, and bleeding from body cavities

Copper Toxicosis

• Chronic accumulation of copper in liver • Ingestion of excess copper in relation to molybdenum or sulfate • Sheep are particularly sensitive to excessive dietary levels of copper • Signs occur when there is a sudden release of a large amount of copper from liver into blood • Stress and liver damage or disease (e.g. flukes) • Excess copper in blood cause rupture of red blood cells = anemia with jaundice (accumulation of bilirubin pigment...turn yellow) • Depression, anorexia, diarrhea, and weakness

Bacillary Hemoglobinuria (Red Water Disease)

• Clostridium haemolyticum • Particularly abundant in pastures with standing water • Colonizes liver and proliferates after liver damage (fluke migration, liver biopsy, etc.) • Produces toxin that destroys red blood cells and causes vascular leakage • Anemia, inflammation of GI tract and kidneys, liver necrosis • Weakness, respiratory distress, fever, jaundice (yellow coloring), and produce red urine and bloody feces • Death in hours to days •Diagnose by isolating organism from lesions • Treatment and prevention as with black disease

Porcine Cystitis-Pyelonephritis Complex

• Cystitis = inflammation of bladder • Pyelonephritis = inflammation of kidney • Most notably due to Actinobaculum suis • Gram-positive, rod-shaped bacterium that grows well under anaerobic conditions • But a wide variety of bacteria has been isolated from cases including Escherichia coli, Streptococcus, and Staphylococcus spp • A leading cause of mortality in sows with increased incidence correlated with use of confinement housing for gestating sows •Reduced frequency of urination and enhanced bacterial survival in urogenital tract due to: •Reduced availability of water • Increased fecal contamination of the perineal area •Excessive weight gain •Leg injuries

Tyzzer Disease in Foals Cont

• Disease in young foals (1-2 wks old) primarily affects liver • Induces a massive multifocal necrosis and hepatitis • Die of acute liver failure, most found in a coma or dead (duration of illness is few hours to 2 days) • If signs = depression, anorexia, fever, jaundice, diarrhea, and recumbency • Older foals (up to 6 wk of age) become more resistant to disease as gut becomes more mature • In other animals, which generally are older when infected, the bacterium affects the intestinal tract and to a lesser extent the liver and heart • Diagnosis with serology of blood, PCR of feces, demonstration of organism in tissue at necropsy •Once C piliforme is present on a farm, it may be seen sporadically year after year •Nearly 100% fatal in affected foals • Few successfully treated cases with IV antibiotics, IV dextrose, and fluids •Where endospores are present in the environment • Many exposed but only immunosuppressed become acutely affected • In general, factors that cause stress and immunosuppression should also be reduced

African Swine Fever cont

• Disease very closely resembles Classical Swine Fever (unrelated viruses) • With virulent strains • Incubation 3-7 days, death within 10 days • Anorexia, fever, incoordination, hemorrhages in skin, vomiting & diarrhea, respiratory distress, and ocular discharge • Morbidity and mortality near 100% • Lesions include hemorrhages in lymph nodes and other organs, fluid in body cavities, meningitis/encephalitis • Those that survive less virulent strains may be persistently infected & have circulating antibody • Do not excrete/transmit virus • Transmitted by ingestion of contaminated pork, direct contact (respiratory secretions, blood), fomites, and soft body ticks •Diagnosis with virus isolation, PCR, or serology •No available vaccination • Prohibit importation of swine and pork products from countries with ASF (also worry about ticks) • All successful eradication programs have involved rapid diagnosis, slaughter, and disposal of all animals on infected premises • Reportable as foreign animal disease

Toxins cont

• Dose is primary concern • Exact intake of a toxicant is seldom known • Duration and frequency of exposure are important • Route of exposure affects absorption, translocation, and perhaps metabolic pathways • Exposure relative to periods of stress or food intake may also be a factor • Environmental factors, such as temperature, humidity, and barometric pressure, affect rates of consumption and even the occurrence of some toxic agents • Ex. mycotoxins and poisonous plants • Various species of animals and strains within species may react differently to a particular toxicant • Variations in absorption, metabolism, or elimination •Nutritional and dietary factors, hormonal and health status, organ pathology, stress, and sex all affect toxicosis • Amount of toxicant required to cause pathology is generally correlated to body weight • However, with greater body weight, a disproportionate increase in toxicity (per unit body weight) of a compound often occurs • Keep records of disinfectants, rodenticides, insecticides used on the premises; medications administered in feed and water; and feed additives • Include material safety data sheets (MSDS) for each chemical used on premises • Samples to be collected for potential analysis in cases of suspected toxicosis include: •Dead or recently euthanized animals that showed clinical signs • Feed and drinking water available when animals were showing clinical signs • Label or picture of product, plant, animals that is suspected to have caused toxicity

Mycotoxins

• Exposure to feed or bedding contaminated with toxins produced during growth of various fungi or molds on cereals, hay, straw, pastures, or any other fodder • Can result in acute or chronic toxicosis • Large variety toxins • Mycotoxic diseases: • Cause may not be immediately identified • Outbreaks are often seasonal • Large numbers of fungi or their spores found on feedstuffs does not necessarily indicate that toxin production has occurred • Absence of molds does not exclude mycotoxicosis (feed storage or preparation conditions can destroy molds while the heat-tolerant mycotoxin persists) •Diagnosis • Presence of a disease documented to be caused by a known mycotoxin • Combined with detection of mycotoxin in either feedstuffs or animal tissues • > 1 mycotoxin may be present • Some mycotoxins are immunosuppressive • May allow pathogens to create a secondary disease that complicates diagnosis • Treatment • Generally not successfully treated with medical therapy after diagnosis • Preventive approach to exposure is preferred

Liver Flukes

• Fasciola hepatica (common liver fluke) • Intermediate aquatic snail host...more common in wet areas • Migration through liver • Anorexia, weakness, anemia, colic, fluid accumulation in abdomen, dry feces, death •Diagnose by identifying eggs in feces or on necropsy • Treatment of herd with flukicides • Prevent by decreasing exposure

Hepatic (liver) Lipidosis

• Fat deposition and accumulation within hepatocytes • Increased fat delivery to and inhibition of oxidation/export from cells • Most often seen in ruminants with metabolic shifts during pregnancy and lactation (blood glucose supply ≠ demand) • Often associated with protein deficiency, starvation, food competition, stress, concurrent disease •Signs include weakness, anorexia, CNS signs (altered ammonia metabolism = hepatic encephalopathy), and death •Confirmatory diagnosis often requires liver biopsy but this may be too stressful for animal • Elevated blood triglyceride and cholesterol levels would support diagnosis but are not present in most cases •Treat with supportive care with focus on providing nutritional support/increasing appetite • Adequate protein intake is particularly important • Limit stress, appetite stimulants [vitamin B, diazepam (i.e. valium)] •Prognosis depends on how early disease is recognized

Tularemia

• Francisella tularensis • Non spore-forming, gram-negative coccobacillus • Killed by heat and proper disinfection but survives for weeks or months in a moist environment • Affects >250 species of wild and domestic mammals, birds, reptiles, fish, and people • Among domestic animals, sheep are most common host • Subspecies F tularensis, associated with type A tularemia • Found predominantly in North America, more virulent • In people, mortality rate up to 30% • Transmitted by aerosol, direct contact, ingestion, or arthropods • Most common vectors are ticks Dermacentor andersoni (wood tick), Amblyomma americanum (lone star tick), D variabilis(American dog tick), and Chrysops discalis(deer fly) •Direct contact with, or ingestion of, infected carcasses of wild animals (eg, cottontail rabbit) • Produce oculoglandular, oropharyngeal (local lesions with regional lymphadenitis), or GI form • Inhalation of aerosolized organisms (in lab or as an airborne bioterrorism agent) can produce a respiratory form • Category A bioterrorism agent

Ergotism Cont

• In pigs • Reduced feed intake and reduced weight gain • Occasionally necrosis of the tips of ears or tail • In pregnant gilts and sows • Lack of udder development with agalactia at parturition (due to an inhibition of pituitary release of prolactin) • Piglets born may be smaller than normal • Most of the litter die within a few days because of starvation •Diagnosis is based on finding causative fungus in grains, hay, or pastures provided to livestock showing signs of ergotism •Control • Immediate change to an ergot-free diet • In pregnant gilts and sows, removal of ergot in late gestation (<1 wk before parturition) may not correct the agalactia syndrome • Animals with clinical peripheral gangrene will not likely recover •Under pasture feeding conditions, frequent grazing or topping of pastures prone to ergot infestation during the summer months reduces sclerotia production

Anthrax Cont

• In ruminants, commonly presents as septicemia with a high fatality rate, often accompanied by hemorrhagic, swollen lymph nodes • Lethal toxin (causes local necrosis) and edema toxin (causes extensive edema) produced by bacteria • Incubation period is 3-7 days • Very acute form (common in cattle and sheep) • Sudden onset, rapid death • Staggering/collapse, respiratory difficulty, trembling/seizures, death • Acute form • Fever with a period of excitement followed by depression, respiratory or cardiac distress, staggering, seizures, and death • Bloody discharge from mouth, nostrils, and anus • Abortion • +/- localized, subcutaneous, edematous swelling of ventral neck, thorax, and shoulders In dogs, humans, horses, and pigs, usually more chronic although still potentially fatal • Although relatively resistant, pigs may develop an acute septicemia after ingestion of B anthracis • Characterized by sudden death, oropharyngitis (rapidly progressive swelling of throat due to inflammation), or more usually a mild chronic form • Rigor mortis is frequently absent or incomplete in animals that die from anthrax • Dark blood may ooze from mouth, nostrils, and anus with marked bloating and rapid body decomposition • Blood fails to clot readily • Hemorrhages throughout body

Photosensitization

• Increased susceptibility of skin to damage caused by ultraviolet light • Photodynamic chemicals accumulate in skin -> stimulated by sunlight on exposed and unpigmented areas -> damage to small vessels by free radicals -> skin necrosis and sloughing • Most common in cattle, sheep, goats, and horses • Time interval between exposure to photodynamic agent and onset of clinical signs depends on: • Type of agent • Dose • Exposure to sunlight

Tularemia Cont

• Incubation period is 1-10 days •Sheep may be subclinically infected or develop septicemia, fever, and respiratory infection • Clinical signs include increased pulse and respiratory rates, coughing, diarrhea, and increased urination with enlarged lymph nodes, liver, and spleen •Death may occur in a few hours or days • Outbreaks in untreated lambs may have up to 15% mortality •Most consistent lesions are white to off-white small foci of necrosis in liver and sometimes in spleen, lung, and lymph nodes Infective dose required to transmit is extremely low • Risk of infection during necropsy or to lab personnel is significant, and special procedures and facilities are essential •Diagnose with culture or serology • Lab personnel should be alerted • Treatment with antibiotics • Control limited to reducing arthropod infestation and to rapid diagnosis and treatment

EIA Cont

• Incubation period of 15-45 days or longer • 3 phases of disease: 1. Acute episode lasting 1-3 days is characterized by fever, depression, and low platelet count 2. Prolonged period associated with recurrent episodes of fever, depression, low platelet count & RBC (anemia), increased heart and respiration rates, jaundice and petechia, epistaxis, muscle weakness, loss of condition 3. In most cases, episodes of clinical disease subside within a year, and infected horses become lifelong inapparent carriers and reservoirs of EIA virus •Diagnosis based on serologic tests • Internationally accepted test is the agar gel immunodiffusion or Coggins test • Can give negative results when collected within first 10-14 days of infection • Reportable disease in NH, testing required for interstate transport •No safe and effective vaccine available •No treatment or cure

SARS-CoV-2 in Mink

• Infections detected in mink in France, Spain, Sweden, Italy, US, Greece, the Netherlands, and Demark • 5 different variant strains of virus have been found in mink • 1 particular variant has been found in human samples too, some from people that are connected to the mink farms, and some from people who aren't • Transmission to cats has been found on mink farms in Netherlands • Denmark is world's biggest mink producer • All 288 infected herds have been killed, ~10 million animals have been culled to date • Denmark's fur industry(~6000 jobs) has almost been wiped out • https://www.wormsandgermsblog.com/

Targeted Selective Treatment (TST)

• Leaves a portion of group untreated • Creates a "refugium" = portion of worm population that was not selected by dewormer treatment • Helps to dilute out resistant genes in nematodes that survive treatment • 30-35% of animals in flock/herd harbor majority of nematodes • Best to target and treat these animals Evaluation of FEC and BCS or determination of reduced weight gain (regular weighing necessary) can be used help select animals to treat • FAMACHA system can help to select animals that need to be treated (those that are anemic/affected by their parasitism) if H. contortus or other hemophagic parasites are a problem • All animals needing deworming 3x more often than group average should be culled • Promote genetic resistance of hosts in group • TST not necessary if being sold for slaughter at a young age (lambs/kids/calves) • Deworming all prior to shipment (with appropriate meat withdrawal time) will put them in better condition without a major concern for promoting resistance

Copper Toxicosis Cont

• Most tissues will be yellow but kidneys are black because of accumulation of other RBC breakdown products •Diagnose by measuring copper in blood or kidneys (liver concentration may be normal after release into blood) • Treatment is usually unrewarding • Fluid therapy, supplemental molybdemum or sulfate, minimize stress • Prevent by feeding 5-10 ppm (parts per million or mg/kg) of Cu in their total diet and less than a 10:1 ratio of copper to molybdenum • If keeping sheep in mixed groups with other animals, be very careful about not overfeeding copper

Classical Swine Fever/Hog Cholera

• Pestivirus, enveloped RNA virus • Highly contagious, virulence of strains varies • Does not persist in environment or spread long distances by airborne route • But can survive curing and freezing in meat • Eradicated from US in 1976 • Occurs only in swine (domestic and feral), all ages susceptible • With virulent strains • Incubation 3-7 days, death within 10 -30 days depending on severity of strain • Morbidity and mortality close to 100% • Depression, anorexia, fever -> huddling, conjunctivitis • Purple/blue skin discoloration (cyanosis) of ears, lower abdomen, and legs • CNS signs (hind limb weakness or paralysis, seizures) • +/-GI signs (diarrhea or constipation, vomiting) • Abortion and mummified fetuses • Low virulence strains • Poor reproductive performance • Piglets with congenital tremor

Iron Deficiency

• Piglets are born with little iron reserve • Colostrum and milk provide relatively little iron • Rapid growth with corresponding expansion of blood volume => nutritional anemia if no supplementation is provided • Especially prone if raised in confinement without access to soil or feces with iron • Pale mucous membranes, enlarged heart, edematous skin around neck and shoulders, weak, with shallow/rapid breathing

Aflatoxicosis

• Produced by toxigenic strains of Aspergillus flavus and A parasiticus on peanuts, soybeans, corn, and other cereals when moisture content and temperatures are sufficiently high for mold growth • Affects growing poultry (especially ducklings and turkey poults), young pigs, pregnant sows, calves, and dogs • Adult cattle, sheep, and goats are relatively resistant to acute form, more susceptible if toxic diets fed over long periods • Metabolized in liver • High dosages cause necrosis of liver cells • Prolonged low dosages result in reduced growth rate, immunosuppression, and liver enlargement • Acute • Death after a short period of inappetence • Vomiting, depression, hemorrhage, and jaundice • Chronic • More common • Unthriftiness, weakness, anorexia, reduced growth and feed efficiency, and occasional deaths • Diagnosis: • Disease history, laboratory data, necropsy findings, and microscopic examination of the liver (could be performed antemortem by liver biopsy) • Presence and levels of aflatoxins in feed should be determined

Snake Bites Lecture Cont

• Prognosis (chance of recovery) depends on: • Type and species of snake • Location of the bite • Size of the victim •Degree of envenomation • Time interval between the bite and the start of treatment • Treatment for crotalid envenomation: preventing or controlling shock, neutralizing venom, preventing or controlling coagulation issues, minimizing tissue necrosis, and preventing secondary infection • Antivenom is the only direct and specific means of neutralizing snake venom • Most effective if administered in the first 6 hr after bite • Bacteria Pseudomonas aeruginosa, Clostridium spp, Corynebacterium spp, and staphylococci have been isolated from the mouth of rattlesnakes • Tetanus antitoxin also should be considered with snake bite cases, especially in horses

Equine Infectious Anemia

• Retrovirus, RNA virus • Worldwide distribution, most common in warmer countries with lots of biting insects • Strains vary in pathogenicity • Readily inactivated by common disinfectants • Of susceptible equids, horses and ponies develop most severe disease • Infected donkeys and mules frequently subclinical • Virus increases production of pro-inflammatory cytokines • Induces fever • Inhibits production of RBC • Causes destruction of platelets (needed for blood clotting) •Usually considered a blood-borne infection • Transmitted mechanically by biting insects and through instruments/needles contaminated with blood • However, all body fluids and tissues should be considered potentially infectious, especially during febrile episodes when viral levels are high • Transplacental transmission also possible

Anticoagulant Rodenticides

• Rodent poison • Interfere with ability of blood to clot • Can also see bioaccumulation if eat animals that ate rodenticide (most common in omnivores like pigs and poultry) • Signs of internal hemorrhage (lungs, intestines, body cavity) • May be able to treat with vitamin K, important to know exact product • To increase protection to nontarget animal species and children, EPA has new rules on packaging and availability of anticoagulants • Restrict type & volume of rodenticides that can be sold direct to consumers • Require that all outdoor, above-ground use must be in a bait station intended to be resistant to children and pets • Loose poison baits (pellets, meals) are prohibited • All outdoor products are to be placed within 50 feet of a building

Ascaris suum

• Roundworm • Most common internal parasite of swine • Reduced feed efficiency • Condemnations of carcasses due to liver "milk spots" • Fecal-oral transmission, life cycle is direct or can pass through earthworm host...zoonotic • Larvae are released in small intestine and migrate across gut wall -> enter circulatory system and travel to liver and lungs -> coughed up, swallowed - > fully mature in small intestine and begin to lay eggs • Infected pigs usually have cough (caused by parasite migration) or are subclinical • Severe cases have stunted growth, diarrhea, and can die of intestinal impaction •Diagnose with fecal flotation to look for ova • Eggs are thick shelled and very resistant (survive up to 7 yrs in environment) • Additional control is through treating with anti- parasitic drugs, washing sows pre-farrow, and pasture management

Cestodes/Tapeworks

• Species vary across mammalian hosts • Segments visible in feces •Usually do not cause clinical disease, except where they are found in very high numbers • Impaired gut motility, anorexia, +/-GI rupture • Life cycle typically includes pasture mite intermediate host like mite • Makes effective treatment difficult

Stephanurus dentatus

• Swine kidney worm • 2-4.5 cm long, adults encyst along ureters and in fat around kidneys • Primarily a parasite of swine raised outdoors in southeastern and south central US • All age groups can become infected, takes up to 10 months for worms to mature in host • Eggs passed in urine • Infection is by skin penetration or ingestion of infective larvae •Damage caused by prolonged (3-9 months) parasite migration to kidneys (condemnation of meat at slaughter) •Diagnosis usually made on post-mortem • Could be made with urine sample •Control • "gilts only" breeding program...worm does not have time to go through whole lifecycle before gilts are sold post-weaning •Deworming

Gapeworms

• Syngamus trachea (in Galliformes) and Cyathostoma bronchialis (in Anseriformes) • Adults nematodes in trachea and lungs • Cough up and swallow eggs • Can cause respiratory distress • Infection is by direct fecal-oral or passage through an intermediate invertebrate host • Can encyst and survive in environment for years

Effective Use of Deworming Drugs

• Target treatment to parasites present in operation and to animals in need of treatment •Use one drug until it fails, then switch to new class • Frequent rotation between classes can hasten development of resistance •Use appropriate dosing • Under dosing can hasten resistance development • Monitor efficacy of treatment with FEC 10-14 days after dosing • Compare untreated group to treated or pre- and post-treatment results from same animal • Pooled fecal samples are not advisable (does not facilitate targeted treatment)

Zearalenone

• Toxin produced by Fusarium spp molds on corn, wheat, and barley • Nonsteroidal estrogen • Potency 2-4 times less than estradiol • Only known mycotoxin with primarily estrogenic effects • Primarily seen in pigs (most sensitive species) but sporadic outbreaks reported in in dairy cattle, sheep, chickens, and turkeys • In pigs, affects weaned and prepubertal gilts • Hyperemia (redness) and enlargement of the vulva (known as vulvovaginitis) • Behavioral signs of estrus • Enlargement of mammary glands and uterus • Abdominal straining results in prolapse of the uterus in severe cases • In sexually mature sows • Causes reproductive toxicosis • Inhibits secretion and release of follicle-stimulating hormone (FSH) = arrest of preovulatory ovarian follicle maturation • Sexually mature sows can retain corpora lutea for 40-70 days after exposure, consistent with signs of pseudopregnancy • Can be excreted in milk • Hyperestrogenic effects in nursing piglets •Young boars and bulls may become infertile, with testicular atrophy •Diagnosis: • Reproductive performance in herd or flock, clinical signs, history of diet-related occurrence, and excluding other known causes of infertility • Chemical analysis of suspect feed for zearalenone • Examination of reproductive organs at necropsy •Usually reproductive functions recover and signs regress 1-4 wk after intake of zearalenone stops • Multiparous sows may remain anestrous up to 8-10 wk

Toxins

• Typically, exposure is through contaminated feed/water or • Too high a dose of an otherwise safe feed/water additive or medicine • Access to poisonous plants, pesticides, and rodenticides • Envenomation (snake, spider, etc.) • Exposure to noxious gases • Topical application • Typically diagnosed based on history of exposure, signs, and lesions on post-mortem • Treated by removing the toxin and providing supportive care (could include assist feedings, fluid therapy, keeping clean and dry) • Potentially lavage or "flush" the GI tract if ingestion was recent • Induce vomiting for some recently ingested toxins, but not recommended in most livestock and/or for caustic substances • If topical, may be recommended bathe animal • Some toxins have specific commercially available treatments or anti-toxins

Bovine Anaplasmosis

• Usually caused by Anaplasma marginale • A. centrale - milder disease • A. ovis - severe disease in deer and small ruminants • Cattle, sheep, goats, and buffalo • Tropical and subtropical regions worldwide, including South and Central America, US, southern Europe, Africa, Asia, and Australia • Transmission = typically tick borne • Dermacentor spp (wood tick, dog tick) main vectors in US • Transplacental transmission has been reported • May also be spread through contaminated needles, dehorning, or surgical instruments •Calves are much more resistant to clinical disease than older cattle: • In animals <1 yr old anaplasmosis is usually subclinical • In 1- 2-yr-olds it is moderately severe • Older cattle it is severe and often fatal • Progressive anemia due to destruction of RBCs • Very acute disease = die within a few hours of onset of signs • Acute disease = lose condition rapidly, milk production falls, inappetence, loss of coordination, increased respiratory effort, fever, rapid bounding pulse, mucous membranes appear pale and then yellow, pregnant cows may abort • Surviving cattle are sick over several weeks, during which RBCs slowly return to normal

Classical Swine Fever

• Vasculitis (causing hemorrhages in multiple organs & cyanosis of skin), encephalitis, lymphoid depletion • Transmitted by direct contact, fomites, arthropods, ingestion of contaminated pork products • Vertical transmission if infected during pregnancy • Diagnose with PCR, virus isolation, or serology to detect antibodies • Reportable in NH (and as foreign animal disease) • Control: • Limiting exposure (biosecurity, quarantine, not feeding/cooking meat scraps, excluding contact with feral hogs) • Strict importation regulations on live swine and pork products • Depopulation and ring vaccination strategy • Note - Currently 28 states and some territories allow garbage feeding • Swine Health Protection Act • Cooked and uncooked product is kept separate so there is no cross contamination. • Equipment used for cooked product is not contaminated with uncooked product. • Garbage is heated to a treatment level of 212°F (boiling) for 30 minutes. • https://www.nationalhogfarmer.com/business/asf-prevention-should-meat-be-removed- garbage-feeding

Snake Bites Lecture

• Venomous snakes of North America are members of either of 2 families: • Elapidae or coral snakes (Micrurus spp) • Crotalidae or pit vipers • Rattlesnakes [Crotalus spp] • Cottonmouth moccasin [Agkistrodon piscivorus] • Copperhead [A cortotrix]) • Only venomous snake native to NH is timber rattlesnake • Endangered species • Livestock typically get bit on tongue, nose, face • Crotalid envenomation • Severe local tissue damage that spreads from bite site • Tissue markedly discolored within a few minutes, and dark, bloody fluid may ooze from fang wounds, if not prevented by swelling • Skin may slough • Neurologic signs possible, mostly muscle twitching • Elapid envenomation • Pain and swelling are minimal • Systemic neurologic signs predominate • Paresis, drooling, rapid shallow breathing, depressed gag reflex, ataxia, muscle twitching, and quiet mentation

Anthrax Final

• Zoonotic disease and reportable • People are relatively resistant to infection • Primarily cutaneous disease (>95% of all cases) • Following contact with contaminated carcasses or animal products • Also • GI anthrax (including pharyngeal anthrax, like pigs get) with consumption of contaminated raw or undercooked meat • Inhalational anthrax (woolsorter's disease) • Highly fatal • Most likely in labs, animal hair processing facilities, exposure to weaponized spore products (category A bioterrorism agent) • WHO estimates 50 kg of B anthracis released upwind of a population of 500,000 could result in 95,000 deaths and 125,000 hospitalizations • Livestock are more susceptible, would result in higher and earlier mortality & morbidity • Injection anthrax has emerged in conjunction with contaminated heroin

Aerosolized Toxins and Poultry

•Ammonia gas • Produced by metabolism of uric acid by bacteria in wet litter • Respiratory irritation, contact burns (skin, corneas) • Recommend <25 ppm to prevent a loss in performance and increase in disease •Polytetrafluoroethylene (PTFE) = Teflon •Used as a coating on heat lamps and space heaters • Toxic if heated >536⁰F •Hemorrhages in the lungs and rapid death

Infectious Bursal Disease

•Birnavirus, non-enveloped RNA virus •Strain virulence varies •Chicks < 3 weeks of age •Atrophy of Bursa of Fabricius • Severe immunosuppression due to destruction of immature lymphocytes • Susceptible to infection by other diseases & do not develop immunity from vaccines • Chicks 3-18wks old • CNS signs, diarrhea, hemorrhages in thigh and pectoral muscles • Bursa is swollen, edematous, +/- hemorrhagic • 100% morbidity, with low mortality (recovery in <1 week) • Transmitted via fecal-oral •Diagnose with PCR • Vaccination will limit early infection and subsequent immunosuppression • Done in chicks and/or in breeder layers (to promote maternal antibody formation)

Porcine Circovirus Diseases (PCVD)

•Circoviridae, DNA virus non-enveloped • PCV Type 2 (PCV-2) most pathogenic • Endemic in US...nearly all swine herds exposed including feral hogs •Transmission •Direct contact with infected bodily secretions and contaminated fomites • Transplacental •Factors influencing disease development: • Age, source, and genetics of pigs • Environmental conditions (stress and sanitation) • PCV strain • Immunologic status of the pig at PCV2 infection "Post-weaning multisystemic wasting syndrome" or PCV2-systemic disease • Nursey and growing pigs • Low to moderate morbidity (5-20%) with high mortality (>50%) • Wasting pigs, enlarged lymph nodes, diarrhea, difficulty breathing • Lymphoid depletion with inflammation in affected organs

Infectious Necrotic Hepatitis (Black Disease)

•Clostridium novyi •Disease of sheep and cattle, rarely seen in horses •Highest incidence in milder, wetter months •Organisms proliferate/produce toxins in liver when fluke migration creates adequate anaerobic conditions there • Flukes may also transmit C. novyi into liver •Necrotic hepatitis •Weakness, anorexia, fever, subcutaneous hemorrhagic edema (more often develops in cattle) •All affected animals die in <1 day •Diagnosed on necropsy and rarely time to treat •Would treat with flukicides, antibiotics, and supportive care •Prevent by controlling fluke infections

Tyzzer Disease in Foals

•Clostridium piliforme •Motile, spore-forming, rod-shaped, obligate, intracellular bacterium •Primary site of infection is lower intestinal tract with subsequent dissemination via blood or lymphatics to liver and heart •Stress factors such as capture, overcrowding, shipping, and poor sanitation appear to be predisposing • Disease in foals more common during spring • Increase in availability of nutrients from pasture forages and supplemental diets may encourage overgrowth of C piliforme in the GI of nursing mares •Foals consume feces of dams soon after birth as a mechanism to establish their normal intestinal flora • Immature gut is likely more permeable to pathogens like C piliforme

Alternative Control Methods Cont.

•Condensed tannin-containing forages • Can markedly decrease viability of larval stages and decrease egg hatching of several nematodes • Particularly good at controlling H. contortus if fed consistently as a high percentage of diet • Also improve protein nutrition in ruminants by binding proteins in rumen (protecting from microbial digestion) and then releasing in abomasum •Nematode-trapping fungi • Produce sticky loop hyphal traps that capture and kill larval worms in environment • Feed fungal spores to host in form that passes unchanged through GI tract but germinate in feces • Waiting on a commercially available product • Vaccines • Lots of research happening, but few products (https://onlinelibrary.wiley.com/doi/full/10.1111 /pim.12398) •Excluding or killing intermediate hosts through insecticide application •Approved antiparasitic medications are rare for poultry (with exception of coccidiostats) and of increasing need for pastured birds • Pumpkin (piperazine compound, mostly in seeds) can be used for roundworms (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037735/) •Diatomaceous earth in feed (<2%) lowers numbers of Heterakis and Capillaria

Urinary Stones in Ruminants

•Development of urinary stones (urolithiasis) and subsequent obstruction of urine flow by these stones is most common urinary tract disease in small ruminants • Also commonly noted in cattle • Stones develop when minerals (calcium, phosphorus, magnesium, etc.) precipitate in urine and form crystals • Increased mineral concentration in diet • Dehydration and/or increased mineral content of water • Abnormal urine pH • Concurrent urinary infection is rare • Stones can be present in any part of urinary tract •Not uncommon for ventral abdominal skin to necrose and slough, allowing a pseudourethra to develop •Diagnosis based on history, clinical signs, and physical examination

Anthrax Conttt

•Diagnosis •Vegetative cell is not robust and will not survive transit to lab • Optimal sample is a cotton swab dipped in blood and allowed to dry • Results in sporulation and the death of other bacteria and contaminants •Pigs with localized disease rarely have bacteria in blood • Small piece of affected lymphatic tissue should be submitted •Tests = bacterial culture, PCR tests, and fluorescent antibody stains •Warn the lab! • Treatment • Long-acting antibiotic, then vaccination ~7-10 days after antibiotic treatment • Simultaneous use of antibiotics and vaccine is inappropriate, because available vaccines for animals in US are live vaccines • Control • Annual vaccination of all grazing animals in endemic areas • Rapid detection of cases with appropriate reporting • Rigid enforcement of quarantine (after vaccination, 2 wk before movement off the farm, 6 wk if going to slaughter) • Isolation of sick animals and removal of well animals from contaminated areas • Suspected contaminated feed should be immediately removed • Treatment of asymptomatic animals after known exposure •Control con't: • Prompt disposal of dead animals, manure, bedding, or other contaminated material by cremation (preferable) or deep burial • Cleaning and disinfection of environment and equipment used on livestock •Use of insect repellents • Control of scavengers that feed on carcasses •Use of PPE when handling diseased animals •Decontaminated soils • Very difficult, formaldehyde will be successful if the level is not excessive • Generally requires removal of soil

Evaluation of Anemia

•FAMACHA score • 5 colors from red (healthy) to white (very anemic) • Match to color of inside of lower eyelid • (FYI = Term is derived from the originator's name...it does not stand for anything) •FAMACHA score correlates well with evaluation of packed cell volume (PCV) •Monitor with FAMACHA evaluation every 2-3 weeks • More often during peak transmission times = warm, humid weather • Especially targeting lambs and kids that lag behind group

Current ASF Outbreak

•Has been found in at least 60 countries on 3 continents since 2016 •Highest impact inAsian countries with 82% of total reported global losses • China • Was home to half of the world's pig population • ASF first reported in China in August 2018 • Have lost or culled millions of animals • Massive effect on international pork market • Price of pork soaring in outbreak countries, which is placing pressure to shift diets (more chicken and beef consumption) • In first ten months of 2020, China imported US$ 25.4 billion worth of meat, an increase of 75% over the previous year • (US pork industry is not benefiting proportionally to China's increase in pork importation because of current tariff/trade war issues) • Also a looming heparin (blood thinner) shortage • Made from pig products and largely sourced from China Especially difficult to trace casing products with skins for sausages/salamis • Typically move through multiple countries • Often cleaned, graded, sorted, treated in different locations • Current legislation pending to fund more agricultural inspectors for customs and border protection • Increasing "Beagle Brigade" • Sniff out pork hidden in luggage at international airports and border crossings • Public education • Feral swine control

Heterakis and Histomonas

•Heterakis gallinarum • Nematode • "Cecal worm" of chickens • Can caused inflammation and necrosis of cecum • Can harbor the worm and be apparently healthy • Earthworms ingest eggs passed in poultry feces and then are eaten by the poultry • Infection highest in the warm, rainy season (when earthworms are most active) • Histomonas meleagridis • Protozoan passed in Heterakis spp. eggs • Released from Heterakis larvae in ceca • Weakness, anorexia, yellow diarrhea, cyanotic head ("turkey blackhead") • Cecal inflammation with ulcerations, necrosis of liver • High mortality in turkeys, high morbidity/low mortality in chickens • No approved, effective treatments in US • Limit contact between turkeys and other Galliformes

Rabbit Hemorrhagic Disease Cont

•Lesions include liver necrosis and hemorrhages in multiple organs (due to clotting issues) •Diagnose by PCR or serology •No treatment, immunity is not cross protective between strains •Vaccines are available •No licensed vaccine for RHDV2 in US • 2 killed vaccines for RHDV2 licensed in EU which may be used in US under special permit/approval of State Vet •Reportable in US as a foreign animal disease

Lungworms

•Many different species in this category •Example Dictyocaulus arnfieldi in equids • Donkeys are definitive host and develop few signs of infection • Horses that share pasture with donkeys or follow them into grazing used by donkeys within a few months are most likely to become infected • Cause bronchitis or pneumonia in horses • Cough, respiratory difficulty, anorexia, weight loss • Predispose to secondary respiratory infections • Severity of disease is related to number of larvae ingested • Infected horses do not produce many infective larvae • Build some natural resistance with infection •Diagnose with fecal flotation or use of Baermann technique • Large fecal samples (25-30 g) are wrapped in tissue paper or cheese cloth and suspended or placed in water contained in a beaker • Water examined for larvae after 4 hr; in heavy infections, larvae may be present within 30 min • Treatment with anti-parasitic medications and move off infected pasture

Alternative Control Methods

•Nutrition • Well nourished animals will tolerate parasitism better...more robust immune response •Mixing livestock species • Most nematodes are host specific...except that sheep, goats, and camelids share many of the same •Grazing horses and cows with small ruminants will help "clean up" the pasture without inducing disease •Pasture rotation • Although rotation every 30 days is often recommended to maintain presence of best forage, also provides for high infective load of larvae to be ready for next group • Recommend rotation every 3 months in hot climates where parasites dry out/die quicker on pastures •Not as effective a strategy in cool/damp climates where they can survive for long periods of time in environment •Genetic resistance in host • Culling animals that are most susceptible (are more heavily parasitized than rest of group/require increased treatment frequency) • Some breeds have demonstrated more natural resistance •Copper oxide wire particles • Effective dewormer against abomasal worms (particularly H. contortus) but not intestinal worms • Be particularly careful if using in sheep because of sensitivity to copper toxicity

Fatty Liver Syndrome in Poultry

•Overfeeding high energy food, limit calorie burn • Most common in caged layers because of their minimal exercise •Geese raised for foie gras •Excessive fat deposition into liver • Enlarges liver, increases friability • Liver capsule can rupture and result in fatal hemorrhage

Parasite Control Programs

•Overuse of anthelmintics (dewormers) has lead to resistance in parasite populations •Once genetic resistance develops, there is no reversion to susceptibility •Need a "whole farm approach" to parasite control

EIA control/prevention

•Prevention & control: • Euthanasia or permanent isolation of EIA-positive horse (lifelong carriers) • Use a sterile needle, syringe, and IV set for all injections or treatments. • Clean and disinfect dental, tattoo, surgical equipment, lip chains, and bits thoroughly between horses • Only administer commercially licensed blood or blood products • Keep open wounds clean and covered, if possible • Require proof of a recent negative EIA test upon introduction of new horses • Practice good fly control

Urinary Stones in Ruminants Cont.

•Treatment involves: •Ensuring a patent stream of urine • Conservative therapy = medications to relax urethra/penile muscles • Surgery often necessary in small ruminants...can remove urethral process but usually have additional stones "upstream" •Removing/dissolving stones • Removal will require surgery • Chemically dissolving stones can be done depending on their composition •Decreasing inflammation in urinary tract •Correcting hydration status •Diagnosis in a single animal suggests that all males in the population are at risk of the disease •Prevention • Provide a 2:1 calcium to phosphorus ratio in diet • Increase water intake -> dilute urine • Maintain urine pH between 5.5-6.5 • Late castration (more testosterone = wider urethral diameter)

Mycotoxins cont

•When mycotoxicosis is suspected: •Change feed • Even when a specific mycotoxin is not identified • Inspect storage bins, mixing equipment, and feeders for caking, molding, or musty odors •Clean equipment and sanitize with hypochlorite (laundry bleach) to reduce contaminating fungi •Analyze for known mycotoxins • Use spore counts or fungal cultures for some indication of potential mycotoxin production • When mycotoxicosis is suspected (con't): •Use a commercially available mold inhibitor to reduce or delay mold growth •Use a mycotoxin adsorbent if appropriate for the mycotoxin suspected • Numerous products marketed as anticaking agents to "bind" mycotoxins & reduce absorption from GI • To date, FDA has not licensed any product for use as a "mycotoxin binder" in animal feeds • Save a representative sample of each diet until animals are at 1 mo beyond when the feed was consumed •Prevention • Testing of suspect feed at harvest • Maintaining clean and dry storage facilities •Using additives (eg, propionic acid) to control mold growth in storage (do not destroy preformed toxins) • Ensuring effective air exclusion in silage storage • Reducing storage time of prepared feeds

Other Deworming Strategies

1. Deworming and then moving to "safe" pastures • Have not been grazed by that species or closely related (sheep/goats) for 3-6 months • Pastures grazed by species that do not share same parasites • Hay pastures or new pastures (those previously used for crops) 2. Till/burn then replant pasture...by time new forage is available, majority of infective larvae will be dead 3. TST deworming as move animals off pasture for winter will help keep parasite burden low during winter 4. Deworming mid-winter with a dewormer that is effective against hypobiotic state (state of arrest that some parasites can go into during times of adverse pasture conditions) of parasite • Reduces number of parasite ova passed onto pasture in spring -These are not effective strategies in mild climates where parasites can overwinter and where hypobiosis is not a major factor 5. Target treatment to times before enter their reproductive phase in hosts • Treatment of animals 10-14 days after a period of heavy rain (particularly if it followed a drought...lots of L3 stage larvae available for ingestion)

Sarcoptic Mange Disease in Camels

1. True or False? Clinical signs of mange disease can consist of itching, hair loss, and anorexia. 2. Sarcoptic Mange in camels can be prevented by doing what? Prevention by using anti-mange mite drugs.

Steroid-responsive Meningitis in Dogs

1. What is the difference between the transmission between bacterial meningitis and steroid-responsive meningitis? Answer: Bacterial meningitis (along with viral) is transmitted through oral and respiratory secretions, while steroid-responsive meningitis is not contagious. 2. What type of diagnostic test will your veterinarian perform on your dog who is experiencing neck pain and decreased blood pressure? a. Bacterial culture b. Serology c. Cerebrospinal fluid (CSF) tap d. CT scan of the shoulders and back

Blackhead Disease in Turkeys (Histomoniasis)

1. What is the most common route of transmission of Blackhead? Ingestion of H. gallinarum (roundworm) eggs infected with H. meleagridis. 2. What are the two pathognomonic signs of Blackhead? Bullseye lesions of the liver and ulceration/yellow caseous exudate in the cecum

Pemphigus Foliaceous

1. What other disease could Pemphigus Foliaceous be mistaken for in the early stages? Rain rot or ring worm 2. What would be your plan for a pony that shows signs of being itchy and having crusty skin on their face and legs? Run a skin biopsy with a fungi stain, then treat with corticosteroids.

Ulcerative Enteritis

1.) Briefly explain how a previous flock of quail infected with ulcerative enteritis could infect a newly formed flock in the same area months later. C. colinum has spores that can live in the environment for months and affect future flocks who haven't previously been exposed to the bacteria. 2.) What is a characteristic lesion of C. colinum ulcers in necropsy examination? A pale yellow halo around the hemorrhagic ulcers in the intestines

Degenerative Myelopathy

1.) Name one breed of dog that is commonly susceptible to DM. German shepherds 2.) True/False: The exact cause of DM is not known

Duck Viral Hepatitis

1.) Name two management practices that can be used to control duck viral hepatitis Pest control, wildlife management, vaccination, etc 2.) How would you definitively diagnose duck viral hepatitis? Viral isolation from liver cells or PCR

Exotic Newcastle Disease

1.) Since END is considered a foreign disease, where should you report to if your flock has been infected with END? The OIE 2.) You notice one morning that almost all of your broiler chickens have dropped dead suddenly even though they showed no signs of illness the previous day. You suspect END as the culprit. How do you confirm this diagnosis? Submit a bird for necropsy to a state laboratory

Gapeworms q

1.) True/False: The nematode once ingested travels through 2 body systems 2.) What is the best way to prevent? A) De-wormer B) Molluscicides C) Keep housing dry D) Housing both adults and young together

Snake Bites

1.) Venomous snake bites in agricultural species may cause CNS, digestive and respiratory symptoms. True/False 2.) Which type of category of posionous venom damages the circulatory system and muscle tissue causing swelling, hemorrhage, and necrosis? Hemotoxic venom

White Muscle Disease

1.) WMD is caused by a deficiency of what vitamin or mineral in a cow's diet? Selenium 2.) Which sample would you collect from a cow to send to the lab if you suspected Selenium deficiency CSF 3.) True/False. The most commonly affected individuals with WMD are adult cows. False

Chlamydia in Koalas

1.) What are two ways that Chlamydia can be transmitted between koalas? Explain how vertical transmission might occur Sexual transmission and mother to offspring. The joey can get chlamydia from consuming the mother's pap in order to be able to digest eucalyptus. 2.) True/False: Antibiotics are generally considered to be an effective and safe treatment for Chlamydia in koalas

Kissing Spines in Horses

1.) Where can kissing spine occur and what does it do to a horse's back? Between T1 - L6 vertebrae and causes bucking, rearing, kicking out, head tossing, back pain, etc 2.) List two possible treatments for kissing spine mesotherapy and corticosteroid injections

Anthrax cont?

1.What animals does anthrax usually infect? Domestic and wild herbivores 2.How do animals contract the disease? Ingesting spores in contaminated soil

Aflatoxicosis Cont

Aflatoxin M1 (principal metabolite of aflatoxin B1) can be detected in urine, liver, kidney, or milk of lactating animals if toxin intakes are high •Dietary levels as low as 10-20 ppb result in measurable metabolites of aflatoxin being excreted in milk • Acceptable regulatory values range from 0.05 - 0.5 ppb in different countries • Aflatoxin residues in organs and dairy products generally are eliminated within 1-3 wk after exposure ends

Coccidia

Eimeria spp. and Isospora spp. • Protozoan parasite, typically species specific • Oocysts can survive for years in damp, dark areas • Fecal - oral transmission • Many animals harbor these parasites • Development of signs related to infective dose, relative pathogenicity of parasite, and host immune response • Typically only those exposed to large numbers (overcrowding) and who are susceptible (young, sick, poor nutrition, stressed) will show clinical signs -Commonly cause of diarrhea • Watery diarrhea with mucus +/- blood • Anorexia, dehydration, rough hair coat, weight loss, decreased feed conversion • Can cause extensive damage to intestine and each species of coccidia prefers to colonize a different portion of intestine • Can cause permanent scarring with chronic decrease in production •Diagnose by clinical signs + identification of large numbers of eggs on fecal flotation • Normal animals can pass small number of oocytes • Treat with supportive care and anti-coccidal drugs •Natural infection produces a species specific immunity (i.e. if infected with a new species of coccidia, animal is not immune) •Control/prevent • Coccidiostats (drugs that interfere with asexual reproduction of organism) added to feed during times of expected stress • Vaccination (if vaccinate, do not use medicated feed too) • Improved management and sanitation

Mycoplasma haemolamae

Gram negative bacteria with no cell wall • Disease of camelids • Attach to red blood cells (RBCs) • Activate inflammatory/immune response • Accelerate destruction of RBCs • Cause anemia and suppression of immune system • Severity of infection waxes and wanes • Increases with stress, heavy GI parasitism, concurrent disease • Signs include progressive lethargy -> collapse, weight loss, and death • 10-20% of all camelids infected • Affects camelids of all ages • Vertical transmission • Biting insects and contaminated needles also likely play a role • Asymptomatic carriers possible • Diagnose by identifying organism in a blood sample or PCR • Can be difficult to diagnose when infection level is low • Treatment with antibiotics (long acting tetracyclines) • May not entirely clear organism, but improves anemia • If immunocompetent, may clear infection on own

White Nose Syndrome (WNS)

How is White Nose Syndrome transmitted? Through direct contact When does White Nose Syndrome affect bats? During hibernation

Fecal Flotation

Identifying eggs in feces microscopically by mixing with solutions that will float eggs out of feces and suspend them • Eggs of different sizes float at different densities, may need multiple solutions • Producers can do this "on farm" •Use to quantify fecal egg count (FEC) to estimate parasite load •However: • FEC not always an accurate indication of number of adult worms present • Can be negative or deceptively low in presence of large numbers of immature worms • Count can be low if egg production has been suppressed by host immune reaction or recent treatment • Variations in egg-producing capability of different worms may also distort the numbers • Identification of certain nematode eggs is impractical except in specialized laboratories • Many of eggs look identical but there are characteristics that can help differentiate larvae of various species • Culture feces to cause larval maturation, 10-14 days •Note that evaluation of a fresh direct fecal smear is needed for some protozoan parasite identification (i.e. Cryptosporidium & Giardia...these are not worm species, you are looking for motile parasites not parasite eggs)

Ergotism

Ingestion of sclerotia of parasitic fungus Claviceps purpurea • Replaces the grain or seed of rye and other small grains or forage plants • Bluegrasses, fescues, and ryegrasses • Cattle, pigs, sheep, and poultry are involved in sporadic outbreaks • Most other species are susceptible • Primarily causes vasoconstriction by direct action on the muscles of the arterioles, repeated doses injures the blood vessels • Initially, reduce blood flow and eventually leads to necrosis of extremities -In ruminants • Lameness, which may appear 2-6 wk or more after initial ingestion • Hindlimbs are affected before forelimbs • Within ~1 wk, sensation is lost in affected part, an indented line appears at limit of normal tissue, and dry gangrene affects distal part • Tip of tail or ears may become necrotic and slough off • Body temperature and pulse and respiration rates are increased • Stimulation of CNS, followed by depression (primarily in sheep)

Newcastle Disease

Like avian influenza, viral strains of ND vary in pathogenicity • Low virulence NDV (loNDV) = lentogenic • Virulent NDV (vNDV) = mesogenic and velogenic (viscerotropic and neurotropic) • Formerly exotic Newcastle disease • Reportable disease • Have occasional outbreaks in US (recent one in California https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-disease-information/avian/virulentnewcastle/vnd), typically with history of exposure to illegally imported fighting cocks &/or backyard poultry • Transmitted primarily by direct contact with infected bodily fluids, but fomite transmission also possible • Clinical signs: • Mild to severe respiratory signs • +/- CNS signs (head tilt, weakness, paralysis) • +/- diarrhea • Death without prior signs (mortality up to 100% with vND) • Impossible to differentiate HPAI from vND by gross examination alone •Diagnose with PCR • Vaccination is possible • Typically combo vaccine with Infectious Bronchitis • Not often performed in backyard flocks, unless known exposure • Potentially zoonotic (conjunctivitis, respiratory disease)